Advancements in agriculture are frequently held back by the prevalence of abiotic stresses. Thus, scientists are continuously attempting to create modern techniques to combat the limits caused. Exogenous protectants are becoming more common for imparting stress resistance (Table 2). Selenium could indeed reduce the likelihood of membrane destruction by enhancing the photosynthetic machinery, increasing the direct quenching of ROS, and boosting enzymatic/non-enzymatic systems that promote plant-based defense through antioxidants (Table 2) [17]. Since Se can perform antioxidant roles in plants, while enhancing crop yield, it is capable of making plants tolerant to several types of abiotic stress. Through a chain of reactions and interactions, Se induces an increase in antioxidant activity and the defense system which strive to maintain plant physiological parameters in their normal state, resulting in a positive impact on crop yield. Several aspects of action by Se, however, remain unknown. Se causes cell death by increasing lipid peroxidation, α-tocopherol concentrations, and, in particular, GPX activity. Thus, systemic defense is strengthened to assist plants in mitigating the effects of ROS and reducing the amount of damage they cause (Fig. 2) [11]. Haghighi et al. [44] investigated Se-absorption and antioxidant-defense reactions in rice, discovering that a small amount of Se (5 mg kg⁻¹) increased the yield and growth of rice by contributing to the functions of glutathione (GSH), ascorbate (AsA), Peroxidase (POD), CAT, and SOD [52]. Under cadmium stress, adding Se (1 M SeO₄²⁻) to the nutrient solution of tomatoes enhanced their functions and antioxidative-defense enzymatics, such as APX (26%) and CAT (21%), thereby improving the ability of tomatoes to tolerate cadmium stress. The GSH biosynthetic pathway was also advanced by Se treatment (33%) [50]. In this regard, treating tomatoes with elemental Se (40 M) resulted in enhanced tolerance to drought and increased activities of SOD (56%), APX (44%), and CAT (27%) [53]. Tolerant plants, treated with Se, reportedly synthesized more antioxidants of the non-enzymatic type, such as α-tocopherol (36%), GSH (107%), and AsA (up to 131%).

Salinity has an impact on agricultural output by impeding plant development and growth. The available literature contains many case studies on the significance of Se in mitigating the adverse effects of salt stress on plants (Table 2). However, there is a lack of sufficient information on how Se mediates the balancing mechanism of plant tolerance to excessive salt.

Numerous tests have been performed to investigate the effectiveness of Se in giving plants the ability to tolerate dry conditions (Table 2). Hasanuzzaman et al. [58] treated rapeseed seedlings with Se (25 μM; Na₂SeO₄) as they were exposed to different drought intensities (10% or 20% PEG). Drought stress had no significant effect on GSH, GSSG, H₂O₂, or MDA accumulation in stressed plants that were treated with Se. Even so, at 10% PEG, there was a rise in the AsA concentration, as well as in the MDHAR and GR activities. Curiously, there were increases in glutathione S-transferase (GST), GPX, DHAR, and Gly I activities under both levels of drought stress, whereas the activities of CAT and Gly II declined [58]. A study on olive plants showed that foliar spraying with Na₂SeO₄ (50 mg or 150 mg Se L⁻¹) increased plant productivity and photosynthetic rates while retaining the RWC at a high level [60]. Particularly, Se promoted the activity of APX, GPX, and CAT, thereby preventing the peroxidation of lipids.

Selenium can inhibit ROS production, increase cellular viability, boost antioxidant activity, and uphold reproductive integrity in vitro and in vivo under extreme temperatures (Table 2). Malerba et al. [73] discovered that Se significantly improved cellular viability by partly preventing the cytoplasm from shrinking, reducing the O₂• output, and ameliorating the effects of heat shock (50°C, 5 min) by controlling the peroxidation of lipids in tobacco cell cultures. Since Se was observed to be involved in defending oilseed rape seedlings from oxidative stress, Hasanuzzaman et al. [11] showed that high temperatures (HT) at 38°C impacted the molecular participants of GSH-AsA biosynthesis, resulting in increased ROS generation [11]. Seedlings supplemented with 25 μM Na₂SeO₄ had more enzymatic activities and managed to accumulate more AsA and GSH. As a result, small supplements of Se caused greater tolerance to oxidative-stress caused by intermittent HT. In small amounts, Se (2 mg L⁻¹ Na₂SeO₄) protected wheat from the damages of HT (38°C). As a spray treatment, Se increased crop growth, photosynthetic pigments, and the total amount of phenols [63]. The growth of cucumber seedlings, their photosynthetic activity and chlorophyll formation were suppressed by HT (40°C/30°C day/night), while the damage caused by oxidative stress became more prominent. However, the use of 8 μM Se at the flowering-initiation phase demonstrated higher photosynthetic rates, more osmolytes, and a greater level of antioxidant activity, thereby defending the crops against oxidative stress and bringing the possibility of optimal yields, compared to the case of untreated crops. Thus, the fruit weight and the total number of fruits per plant increased by 43% and 35%, respectively, in Se-treated crops, especially in comparison with HT-treated crops without the Se treatment [64].

Selenium partially helps protect crops from the effects of low temperatures (LT). A dose-dependent application of Se assisted cucumbers in becoming less prone to chilling-injury [74]. When exposed to LT, Se-treated cucumber plants showed resistance to the kind of oxidative stress that resulted from LT. Iqbal et al. [75] discovered that Se largely exerts its effects depending on the dose of the treatment, with a negative effect at larger doses. Responses of wheat seedlings to exogenous selenium supply under cold stress. They discovered that applying Se at 0.5 or 1.0 mg kg⁻¹ enhanced chlorophyll content and seedling biomass, whereas its dose at 2.0 and 3.0 mg kg⁻¹ enhanced the amount of chlorophyll only. Furthermore, the effectiveness of antioxidant activity varied in response to high or low levels of Se application, although it was reported that the 1.0 and 2.0 mg kg⁻¹ dose was partly successful in mitigating the effects of LT on lipid peroxidation. Huang et al. [15] discovered that using Se treatments as a foliar spray reduced the adverse impact of LT on strawberries. In a time-dependent manner, while photosynthetic parameters were rendered suboptimal because of chilling-stress, and as the antioxidant activity of enzymes decreased, the role of supplementary Se (5 mg L⁻¹) improved the condition of LT-affected plants, compared to the control group.

The physiological performance of various plants reportedly increased in response to Se application, as they demonstrated enhanced levels of resistance to toxic levels of metals and metalloids (Table 2). Se has reportedly protected plants by causing the roots to reduce their absorption of metalloids and metals that may become toxic, limiting the extent to which they are mobile in reaching aerial organs of plants [39]. When Se is added to heavy metal-containing media, it may come into contact with the subcellular distribution and chemical variants of heavy metals that enter the roots and with the elements in the cellular walls of roots [76]. Surprisingly, Se creates an encouraging scenario for Fe absorption, invigorating the roots to absorb more of it, and, thus, providing more for the requirements of photosynthesis and chloroplast-driven processes [39]. Furthermore, when plants gain access to supplementary Se, they become more capable of synthesizing phytochelatin (PC) and compounds that can counter toxicity. Se can bind to other metals and form complex molecular structures that aid in the reduction of toxic symptoms caused by unwanted metals/metalloids [66]. In a relevant study, Se (2 μM) reduced the toxic effects of cadmium in oilseed rape by regulating, CAT, SOD, GPX, and APX activities and limiting the peroxidation of lipids [68]. In a report it was shown that Se had a significant role in reducing MDA-based substances, while enhancing the activities of MDHAR, APX, GR, DHAR, CAT, and GPX in plants, increasing the amounts of GSH and AsA, and leveling up the GSH/GSSG ratio in Cd-stressed oilseed rape [11]. Se contributes to the suppression of cadmium translocation, making it difficult for this element to reach the aerial parts of plants and hampering its bioavailability to plant cells [66].

Applying exogenous SeO₃²⁻ (5, 10, and 15 mg kg⁻¹) significantly reduced the accumulation of lead- and cadmium-based compounds in rapeseed, and, ultimately, hampered the mobility of these compounds in the xylem [77]. Furthermore, SeO₃²⁻ reduced the amount of oxidative damage caused by cadmium and lead, through the discouragement of ROS production and lipid peroxidation. In faba beans, lead-induced stress was countered by small supplementary quantities of SeO₃²⁻ (1.5 or 6 μM) [46].

According to Cartes et al. [42], SeO₃²⁻ has been effective in neutralizing the toxicity of aluminum (Al) in ryegrass roots. It was discovered that Se contributed to the increase in POD activity, along with greater O₂^•− dismutations into H₂O₂, but it significantly reduced the output of thio-barbituric acid-reactive substances (TBARS). SeO₃²⁻ functioned as an efficient neutralizer of toxic metals by promoting the synthesis of GSH and thiols, while decreasing the peroxidation of lipids [42].

The most fundamental biological procedure in crops is photosynthesis. Se is capable of boosting antioxidant activity through enzymatic pathways, thereby helping plants defend themselves from stressful conditions. Enzymes of antioxidant capacity include, but are not limited to, peroxidase, catalase, glutathione peroxidase, superoxide dismutase, and ascorbate peroxidase [79–81]. Selenium-based compounds have been shown to stimulate biomass production and boost photosynthesis in lettuce and sorrel plants [82]. Of this kind, selenium-based compounds benefited the physiological aspects of barley and sorghum [61]. The normality of photosystem attributes was reportedly maintained by the application of selenium, protecting plants from the adverse effects of UV-B radiation and cadmium [83]. Selenium influenced the expression of photosynthesis-related genes. In potato leaves, selenite made a transient repression of genes encoding light-receptive compounds involved in photosynthesis [84]. From a perspective of proteomics, selenium treatments had a significant impact on rice crops, their primary metabolism, photosynthesis, and redox homeostasis. Selenium deficiency activated the anti-oxidative system, enhancing photosynthesis and primary metabolic activity. Applying high Se concentrations, on the other hand, harmed the photosynthetic apparatus, inhibited photosynthesis, and suppressed primary metabolic activity. Variations exist among the responsiveness of different genes to selenium [85]. Relevant research indicated that spraying amino acid, chelated-selenium on pears, grapes, and peaches increased their photosynthetic output. Precisely, the efficiency of PSII was enhanced by the application of supplementary Se which, in turn, promoted photochemical quenching [84].

Selenium-induced dysfunctions are likely to have adverse impacts on photosynthesis, suggesting preliminary causes of excessive ROS buildup and oxidative pressure [39]. However, regarding the anti-phytotoxic roles of Se, Meeta et al. [86] discovered that 0.1–0.5 μM of SeO₃²⁻ reduced cellular levels of aminolevulinic acid (ALA) in maize foliage [86]. Relevantly, a decrease in chlorophyll content was significantly notable compared to the decrease in carotenoid compounds and ALA. Nonetheless, providing plants with more SeO₃²⁻ resulted in a reduction of ALA buildup in the presence and absence of light. Based on the available data on growth inhibition, chlorophyll decreased significantly in cucumber plants that faced Se-deficiency [87]. As a result, a decline in photosynthetic pigment concentration levels is viewed as a more prevalent response to the phytotoxic effects of high-dose Se, whereas leaf area and FW seem to be affected less intensely. Zhang et al. [88] demonstrated in an experiment that SeO₃²⁻ levels greater than 50 g.ha⁻¹ decreased rice yields by affecting the photosynthetic integrity of plants while also disrupting their chlorophyll fluorescence [88]. With an abundance of Se-based supplements, the PSII was mostly suppressed because of abnormal changes in Fv/Fo and Fv/Fm ratios, resulting in a decrease in maximum quantum yield, a limited ability to uphold the normality of PSII functions, associated with a loss of thylakoid-membrane integrity [89]. Indicated ultrastructural adjustments, and chloroplast modifications, with a loss of appressed domains, due to the fact that toxic levels of SeO₄²⁻ destabilize chloroplasts [89]. In effect, electron transport chains are inhibited by such toxic levels. Cell size, cellular activity, and maintenance are all involved in rendering photosynthesis optimal. Compared to the regulation of plant development, the normality of photosynthetic activity is more susceptible to Se toxicity. Excess amounts of Se-based compounds can disrupt the appropriate ratios of necessary minerals in crops, thereby instigating unwanted fluctuations in the availability of nutrient contents in plant cells. Se ions can interfere with the regularity of nutrient levels, destabilizing the physiological functions that they control. The interplay between Se and essential elements is proportional, resulting in synergistic and antagonistic impacts. In maize, the application of SeO₃²⁻ (5–100 μM) led to high levels of calcium and phosphorus in the aerial parts of plants, whereas potassium was reduced [90]. Furthermore, Gui et al. [69] discovered that SeO₃²⁻ (10–100 mg kg⁻¹) suppressed the activity of roots in absorbing K, P, magnesium (Mg), copper (Cu), arsenic (As), and zinc (Zn) in Chinese brake fern (Pteris vittata L.). Se-based compounds reportedly altered the coefficients of permeability for certain ions, influencing their ability to cross membranes [91]. In contrast, some plant species cannot accumulate Se because Se-based amino acids fail to be replaced specifically with other viable Se equivalents. As a result, Se-susceptible crops incorporate Se into their protein structures, and, thus, render the proteins dysfunctional. In contrast, Se-tolerant species avoid incorporating Se into their proteins. Two amino acids are Se-based, i.e., selenocystathione and methylselenocysteine, which are normally not incorporated into protein structures in Se-susceptible species [92]. In Arabidopsis, the application of SeO₃²⁻ led to cellular membrane adjustments and regulatory changes in stomatal behavior. SeO₃²⁻ decreased the number of stomata in the leaves and instigated an intense condition of oxidative stress, as well as a medium degree of nitrosative stress [28]. Brassica juncea, on the other hand, responded to SeO₃²⁻ by opening the stomata and accumulating more pectin. As a result, the plants developed severe nitrosative stress and a medium level of oxidative stress. The authors proposed that resistance to SeO₃²⁻ partly emanates from the ability of plants to control oxidation processes. Kolbert et al. [93] demonstrated that the toxic effects of Se target crop proteomes, and, thus, result in the formation of not just oxy- and seleno-proteins, but nitro-proteins as well [93]. Crops that withhold Se-Cys from protein biosynthesis could indeed reduce Se-induced proteomic damages. Proteasome compounds are capable of removing old or deformed selenoproteins, nitroproteins, and oxyproteins.

Se has key roles as a macronutrient in a wide range of organisms, although at high concentrations it can impede gene expression. While plants respond variedly to Se, supplementary amounts of Se are generally required to compensate for Se-deficient conditions. Other treatments may contribute to the cleaning up of Se-polluted soils. Plant hormones, e.g., salicylic acid, ethylene, and jasmonic acid, are tasked with triggering Se resistance and, according to biochemical and molecular research, aiding non-accumulator crops in their tolerance to Se toxicity. Non-accumulator crops are plants that cannot accumulate Se; otherwise, they will suffer from physiological dysfunctions. As phytohormones are generated, tolerance to Se toxicity is aided by processes that enhance ROS scavenging, as well as phytohormones that coordinate an appropriate amount of Se-uptake. When Se-rich soils become saturated with moisture, selenate becomes more likely to permeate shallow aquifers [94]. High levels of Se absorption from the soil profile can sometimes be perilous for animals and humans if they regularly include Se-affected plants in their diet [95]. Due to the chemical similarity between sulfur (S) and Se, sulfate transporters in plant cells may take up Se along with S and, even worse, integrate Se into the structure of methionine (Met) and cysteine (Cys) analogs, as well as seleno-Met (SeMet) and seleno-Cys (SeCys) [96]. Substitutions of important S amino acids, i.e., Met and Cys in proteins, with Se-analogs, can become lethal to plant cells because they restrict S bridge forming and/or distort protein formulation [97]. A significant portion of studies on Se-resistance elaborated on how S interacts with Se whenthe former is metabolized in plants. Based on recent findings, Se induces responses in the defensive system, often reacting hypersensitively to abiotic and biotic stressors [98]. An interplay between several induced responses forms an integral part of Se-resistance in both accumulator and non-accumulator crops [99]. A complete evaluation of Se-receptive gene clusters in A. thaliana, a non-accumulator species, revealed the participation of defensive phytohormones in imparting Se-resistance to plants. In fact, transcriptome analyses have been aimed at recognizing selenate-receptive gene clusters. Treating plants with appropriate amounts of selenate increased the rates at which jasmonic acid (JA)- and ethylene-responsive genes were expressed [100]. Furthermore, extensive amounts of analyses on gene expression revealed that most of these responsive genes were induced in crops treated with selenate [98]. Specifically, Se-treated plants showed a greater level of induction for several genes, i.e., pathogenesis-related 4 (At3g04720, PR4), ethylene response factor 1 (At3g23240, ERF1), vegetative storage protein 1 (At5g24780, VSP1), plant defense in 1.2 (At5g44420, PDF1.2), JA-responsive gene (At3g16470, JR), and proteinase inhibitor 2 (At2g02100, PIN2) [98]. Furthermore, important enzymes were expressed in larger amounts by genes responsible for the synthesis of 1-aminocyclopropane-1-carboxylate synthase 6 (At4g11280, ACS6), S-adenosyl-Met synthase (At1g02500, SAM), and ethylene [101], in addition to allene-oxide synthase (At5g42650, AOS) and lipoxygenase 2 (At3g45140, LOX2) genes. These were reportedly involved in JA biosynthesis [98]. Relevant findings indicated that JA and ethylene production rates usually differ in response to Se-treatments. Exogenous selenite increased the accumulation of JA and ethylene molecules less significantly in a selenite-susceptible accession ‘Ws-2’, compared to a selenite-tolerant accession ‘Col-0’ [102]. Thus, it can be inferred that Se-tolerance can be induced with the help of JA and ethylene in non-accumulator plants. The role of JA and ethylene in Se-tolerance has been explored in non-accumulators while considering their biosynthetic pathway or signaling. Mutations were identified in the Se-tolerant accession ‘Col-0’, in its acs6 locus which lacked ethylene-producing signs due to a mutation in the ACS6 gene. Also, there were mutations in ein2 which caused a lack in ethylene-signaling [103] and jar1 which lacked the ability to synthesize standard JA after the mutation [104]. The above mutants seemed to be more susceptible to selenate and selenite, compared to the susceptibility of the wild Col-0 genotype [105]. In contrast, a test was conducted on ‘Ws-2’, as a susceptible accession, to determine whether cellular tolerance to selenite was restricted by smaller amounts of JA buildup and ethylene release. The results demonstrated that the provision of MeJA or 1-amino-cyclopropane-1-carboxylic acid (ACC, an ethylene precursor) increased cellular tolerance to selenite in the ‘Ws-2’ accession [98]. Such findings implied that ethylene and JA are able to contribute to Se-tolerance in plants. Some other defensive patterns reportedly involved phytohormones and salicylic acid (SA) which accumulated in selenite-treated A. thaliana [106]. Among the phenylpropanoids, the biosynthesis of SA is triggered by various biotic and abiotic stressors [107]. In A. thaliana, isochorismate-synthase 1 (ICS1) encoded an enzyme that limited the rate of SA biosynthesis [108]. Higher amounts of SA accumulated in plant cells and the ICS1 gene was expressed more in response to exogenous selenite. This was observed in the Se-resistant accession ‘Col-0’ and also in the Se-susceptible accession ‘Ws-2’ [109]. In some cases, mutations in SID2 and NPR1 genes have reportedly hampered the biosynthesis and signaling of SA, respectively [110]. Nonetheless, no significant variation was observed in selenite tolerance, compared to the non-mutant genotype, ‘Col-0’, which is an Se-tolerant accession. Even so, using SA on these plants made them more susceptible to selenite [109]. In comparison with the role of JA and ethylene, Se-tolerance is rather suppressed by accumulated amounts of SA in plants. The exact mechanism of SA’s negative impact on Se-tolerance still seems unknown, but an interplay among JA, ethylene, and SA signaling can be a plausible cause. In fact, relevant research on phytohormones revealed their effective role in relieving biotic and abiotic stress in crops, possibly through a mutually antagonistic or coordinated manner. Regarding A. thaliana, many recent genetic experiments have shown that SA can affect JA-signaling antagonistically. For example, pad4 and eds4 mutants lacked accumulated amounts of SA, and, thus, responded favorably to elicitors of gene expressions dependent on JA [111]. Mutations in several JA-signaling proteins, suppressors of SA insensitivity2 (ssi2), kinase4 (mpk4), and coronatine insensitive1 (coi1), on the other hand, demonstrated that JA-signaling antagonizes the appropriate regulation of SA-related defense lines in A. thaliana [112]. Accordingly, SA is thought to suppress the action of ACC oxidase for the complete process in ethylene synthesis [113]. The suppression of SA signaling pathways via ethylene has been proven by transcriptome analyses and mutants that are not sensitive to ethylene [98]. Experimentally, enhanced Se-sensitivity can be associated with the existence of SA and could be mediated by the suppression of ethylene and JA-signaling pathways.